ArticleJournal of medical toxicology : official journal of the American College of Medical Toxicology2024
Investigation of Cerebral Mitochondrial Injury in a Porcine Survivor Model of Carbon Monoxide Poisoning.
Article in Journal of medical toxicology : official journal of the American College of Medical Toxicology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 4 citations in OpenAlex.
- Hypocapnia in acute carbon monoxide poisoning: A complex interaction beyond metabolic compensation.PloS one · 2026Article
- Extreme Cold Events and Pediatric Asthma Outpatient Visits: The Modifying Role of Ambient Carbon Monoxide and Sulfur Dioxide.Journal of asthma and allergy · 2026Article
- Carboxyhemoglobin: a potential participant in neonatal hemolytic jaundice accompanied with myocardial injury.European journal of medical research · 2025Review
- Blood Cells as a Cellular Biomarker for Mitochondrial Function in a Experimental Model of Acute Carbon Monoxide Poisoning with Treatment.Journal of medical toxicology : official journal of the American College of Medical Toxicology · 2025Article
- Carbon monoxide as a cellular protective agent in a swine model of cardiac arrest protocol.PloS one · 2024Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
introductionCarbon monoxide (CO) is a colorless and odorless gas that is a leading cause of environmental poisoning in the USA with substantial mortality and morbidity. The mechanism of CO poisoning is complex and includes hypoxia, inflammation, and leukocyte sequestration in brain microvessel segments leading to increased reactive oxygen species. Another important pathway is the effects of CO on the mitochondria, specifically at cytochrome c oxidase, also known as Complex IV (CIV). One of the glaring gaps is the lack of rigorous experimental models that may recapitulate survivors of acute CO poisoning in the early phase. The primary objective of this preliminary study is to use our advanced swine platform of acute CO poisoning to develop a clinically relevant survivor model to perform behavioral assessment and MRI imaging that will allow future development of biomarkers and therapeutics.
methodsFour swine (10 kg) were divided into two groups: control (n = 2) and CO (n = 2). The CO group received CO at 2000 ppm for over 120 min followed by 30 min of re-oxygenation at room air for one swine and 150 min followed by 30 min of re-oxygenation for another swine. The two swine in the sham group received room air for 150 min. Cerebral microdialysis was performed to obtain semi real-time measurements of cerebral metabolic status. Following exposures, all surviving animals were observed for a 24-h period with neurobehavioral assessment and imaging. At the end of the 24-h period, fresh brain tissue (cortical and hippocampal) was immediately harvested to measure mitochondrial respiration.
resultsWhile a preliminary ongoing study, animals in the CO group showed alterations in cerebral metabolism and cellular function in the acute exposure phase with possible sustained mitochondrial changes 24 h after the CO exposure ended.
conclusionsThis preliminary research further establishes a large animal swine model investigating survivors of CO poisoning to measure translational metrics relevant to clinical medicine that includes a basic neurobehavioral assessment and post exposure cellular measures.
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